Anaemia

Anemia
Anemia is a reduction in O2 transporting capacity of

blood, due to reduction of total circulating red cell
mass to below-normal amounts.
- Robbins
Anemia is defined as a Hb concentration in peripheral

blood below normal for age & sex of patient.
• Hb < than
• 13gm/dl in adult males,
• 11gm/dl in adult females
• RBC count < 4 million/cumm blood

Classification
• Based on
1) Pathogenesis and Etiology (Whitby’s)
• Increased blood loss
• Impaired red cell production
• Increased destruction of red cell.
2) Morphological ( Wintrobe’s)
 Anemia due to Blood loss
• Acute post hemorrhagic anemia

• Chronic post hemorrhagic anemia
 Impaired red cell production
a) Cytoplasmic maturation defects:

1. Deficient haem syn. – iron deficiency anemia
2.Deficient globin syn. – thalassaemia
b) Nuclear maturation defects : Vitamin B12 and/or folic
acid deficiency – megaloblastic anemia
Impaired red cell production cont…
c) Defect in stem cell proliferation & differentiation :

Aplastic anemia
d) Anemia of chronic disorders: eg. inflammation,
infections, renal diseases, endocrine disorders and liver
disease
e) Bone marrow infiltration - leukemia, lymphoma,
multiple myeloma
f) Congenital anemia: sideroblastic anemia
Increased red cell destruction - Haemolytic
anemia
a) Extrinsic red cell abnormality - acquired hemolytic

anemia
b) Intrinsic red cell abnormality - hereditary anemia
Morphologic Classification (Wintrobe’s)
 Normocytic Normochromic
(MCV 76-96fl, MCHC 30-35gm/dl)
 Microcytic, Hypochromic
( MCV< 76 fl, MCHC<30gm/dl)
 Macrocytic (MCV>96fl)
Normochromic Hypochromic
Normocytic •After acute hemorrhage After chronic
•All hemolytic anemia hemorrhage
except thalassemia
•Aplastic anemia
Macrocytic All megaloblastic anemia Secondary to liver

disease
Microcytic Chronic infections •Iron deficiency

anemia
• Thalassemia
General Symptomatology of Anaemia
• Symptoms & Signs – due to resulting tissue hypoxia

& compensatory mechanisms
• Tiredness, easy fatiguability & muscle weakness –
muscle hypoxia
• Pallor – palmar crease, oral mucous membrane, nail
bed & palpebral conjunctiva due to ⇣Hb &
redistribution of blood flow
• RS - Dyspnoea – compensatory
• CVS - Palpitation, tachycardia, cardiac murmurs
• CNS – due to cerebral hypoxia - dizziness, headache,
fainting, tinnitus, vertigo, irritability

• Ocular – visual disturbances
• GIT – nausea, anorexia , indigestion, bowel irregularity
• Menstrual disturbances
• BMR - increased
Iron Deficiency Anaemia
Causes of Iron deficiency Anaemia
1) ↓D Intake - food fads, old age, poverty.

2) ↓D Absorption - achlorhydria, gastric surgery,
intestinal disorders (chronic diarrhoea, sprue
malabsorption)
3) Iron Loss (Bleeding) - Peptic ulcers, Hemorrhoids,
Ca Colon, Hookworm, VWD, Platelet disorders,
Genito-urinary, Pulmonary haemorrhage, Uterine
bleeding
4) ↑ Requirement - Infancy, Pregnancy, Lactation.
Clinical picture of iron deficiency
• Pallor – Palmar crease, tongue, nails conjunctiva,
KOILONYCHIA – dry, brittle ,Spoon shaped Nail (Slow
growth of Nail plate)
GLOSSITIS – Red, Swollen, Angular stomatitis
Smooth, Shiny, Tender (Cheilosis) – fissuring &
Fissured tongue ulceration at the corner of
mouth
• Gastric atrophy with Achlorhydria
• Oesophagus – membranous web at post crycoid web
leading to dysphagia (PLUMMER WILSON SYDROME)
• PICA – Starch (Amylophagia), Clay (Geophagia) Starch,
Clay bind iron, worsening iron deficiency
Investigations
Blood picture and red cell indices:
• Hemoglobin: fall in hemoglobin concentration
• Reticulocyte count: normal or reduced but
may be slightly raised (2-5%) in cases after
hemorrhage.
• Absolute values:
Diminished MCV (below 50 fl)
Diminished MCH (below 27 pg)
Diminished MCHC (below 30g/dl)
Treatment of iron deficiency anaemia
1) Investigate & Remove the cause

2) Iron Supplements:
• Oral – 325mg tablet of Ferrous Sulphate / Gluconate/ Lactate
60mg elemental Iron thrice daily after food.
• IM – Test dose of 50 mg, then upto 2gm – Z tract to prevent
oozing into dermis. In emaciated patients, IV 500 mg in 50 ml
distilled water slowly.
Megaloblastic anemia
• Abnormal large cells of erythroid cells
• Defective DNA synthesis - Vit. B12/ Folic acid deficiency.
• Causes of Cobalmin deficiency
• Decrease intake (vegetarians) – Rare
• Malabsorption –
Folic acid deficiency
• Inadequate intake- Alcoholics – interferes with

folate metabolism
• ↑Demand- Pregnancy, infancy, lactation,
adolescence,
• Malabsorption
• Drugs
Clinical features of cobalmin deficiency
1. Weakness, vertigo, tinnitus, palpitation, rapid pulse,
enlarged heart, systolic flow murmur, purpura.
2. GIT – Tongue – red, smooth, diarrhoea, anorexia
3. CNS – sub acute combined degeneration of sp cord
Demyelination
of posterior &
lat column
Clinical features of folic acid deficiency
1. Haematological manifestation
2. Cheilosis, Glossitis
3. Diarhoea
4. NO NEURONAL ABNORMALITIES
Diagnosis
1. Hemoglobin level reduced

2. Macrocytosis MCV>100FL, normochromia
3. Reticulocyte (>5%),
4. ↓ WBC count, ↓ platelet count. (encroachment)
5. Marrow – megaloblastic hyperplasia
Marrow iron – inc in number & size of granules
Management of VitB12 & Folic acid
deficiency
• B12 Deficiency
– Cause usually not remediable
– Oral therapy usually not appropriate
– Parenteral B12 1000µg / wk 8 weeks
1000µg / months
– Maintenance for life
• Folic acid deficiency

– Remove / modify cause
– Oral therapy 1-5 mg / Day
Pernicious Anemia
(Addisons Anemia)
• Atrophy of gastric
mucosa resulting in
failure to secrete
‘INTRINSIC FACTOR”.
Clinical features
• Rare before the age of 30yrs increasing in frequency
with advancing age.
• Males > Females.
• Triad of symptoms present are:
– Generalized weakness.
– Sore painful tongue(beefy)
– Numbness / Tingling of extremities.
• Lingual manifestations may be first sign in some cases.
 Achlorhydria / lack of HCL secretion.
 pH of the gastric contents is usually high.
 Associated with the atrophy of the gastric mucosa.
 Atrophic gastritis is related to gastric carcinoma.
Incidence is between 5-10%.
APLASTIC ANAEMIA
Aplastic anaemia
Pancytopenia with bone marrow hypocellularity.
Anaemia could be congenital or acquired
CAUSES OF ACQUIRED APLASTIC ANAEMIA
I. RADIATION
II. CHEMICALS – Benzene
III. DRUGS- Chloramphenicol & other antibiotics,
Antiprotozols – Chloroquins, NSAID,
Sulfonamides, Insecticides. Heavy Metals – Gold,
Hg., Allopurinol
Clinical features of aplastic anaemia
1. Anaemia
2. Bleeding – Nose, Skin (Petechiae), GIT, Gums,
haematuria, intracranial haemorrhage, Retinal.
3. Lassitude, weakness, Shortness of Breath.
4. INFECTION – Pharyngitis, anorectal infection,
cellulitis, oral necrotic ulcers, sepsis elsewhere,
septicemia.
HAEMOLYTIC ANAEMIA
Haemolytic anaemia
Premature, ↑ed destruction of RBC, bone marrow
capable of responding.
Classification
I. INTRACORPUSCULAR DEFECTS (Usually Inherited)

1) RBC membrane defect
− Spherocytosis, Elliptocytosis
2) Haemoglobinopathies
− Sickle cell disease, Thalassemia.
3) Enzyme deficiencies
− G6PD, Pyruvate kinase, Hexose kinase
deficiency.
II. EXTRA CORPUSCULAR DEFECT
A. Entrapment (Acquired)- Hypersplenism
B. Immune haemolytic anaemia
− Warm reactive (IgG) antibody.
− Cold reactive IgM antibody (Cold agglutinin
disease)
C. Traumatic haemolytic anaemia
− Macro vascular defects – Prosthesis
− Micro vascular causes – TTP, DIC
D. Haemolytic anaemia due to toxic effects on
membrane- External toxin – Animal bites, metal
Hereditary spherocytosis
• Spherical shape - Defect in protein on RBC

membrane (AD inheritance)
• ↓SA / volume ratio
• ↓ Ability to take up H2O . Lyse at higher NaCl conc.
(osmotic fragility test)
• Because of shape of rigidity hemolysis occurs ↓life
span Spherocytes
• Loss of central pallor
G6 PD Deficiency
• Gene for G6PD on x chromosome deficient

• Glu-6-phosphate dehydrogenase – for formation of
NADPH which maintain glutathione in reduced state
• No G6PD No NAPDH  ↓ed reduced Glutathione
 damage to RBC membrane
SICKLE CELL ANAEMIA.
CAUSE
??
When RBC release

oxygen, hemoglobin
becomes rigid,
stretching the cell
into the
characteristic sickle
CLINICAL FEATURES
• Pain in bones, Precipitation with infection,
dehydration, hypoxia etc
• Shortened cell survival
• Chronic hemolysis
• Splenic sequestration – infarction
• Marrow aplasia.
• Avascular necrosis of hip/shoulder/vertebrae
• Pulmonary hypertension
• Leg ulcers
• Cardiomegaly/cardiomyopathy/MI
• TIA’s/fits/stroke
• Cholelithiasis – pigment stones
Clinical Presentation
Investigations
• Hemoglobin level: 6-8 gm/dl

• Peripheral film – normochromic, poikilocytosis, sickle
cells
• Hb Electrophoresis
• No HbA
• Unconjugated bilirubin.
• Newly born screening.
• Prenatal diagnosis.

Anaemia

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Anemia

Anemia is a reduction in O2 transporting capacity of

Anemia is defined as a Hb concentration in peripheral

• RBC count < 4 million/cumm blood

• Acute post hemorrhagic anemia

a) Cytoplasmic maturation defects:

c) Defect in stem cell proliferation & differentiation :

a) Extrinsic red cell abnormality - acquired hemolytic

Macrocytic All megaloblastic anemia Secondary to liver

Microcytic Chronic infections •Iron deficiency

• Symptoms & Signs – due to resulting tissue hypoxia

fainting, tinnitus, vertigo, irritability

1) ↓D Intake - food fads, old age, poverty.

1) Investigate & Remove the cause

• Inadequate intake- Alcoholics – interferes with

1. Hemoglobin level reduced

• Folic acid deficiency

I. INTRACORPUSCULAR DEFECTS (Usually Inherited)

• Spherical shape - Defect in protein on RBC

• Gene for G6PD on x chromosome deficient

When RBC release

• Hemoglobin level: 6-8 gm/dl

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